Key Laboratory of Molecular Cardiovascular Diseases

Beijing, China

Key Laboratory of Molecular Cardiovascular Diseases

Beijing, China
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Liao Y.,Peking University | Mi J.,Capital Institute of Pediatrics | Wang Y.,Peking University | Chen S.,University of California at San Diego | And 6 more authors.
Pediatrics International | Year: 2010

Background: The present study was designed to explore the reference values of serum lipids in children in Beijing. Methods: A total of 1071 healthy children from Beijing between 3 and 18 years of age were enrolled and divided into four groups: A, 3-5-year-old group; B, 6-9-year-old group; C, 10-14-year-old group; and D, 15-18-year-old group. Blood samples were obtained from the cubital veins of the participants under a fasting condition. A Hitachi 7600 Automatic Biochemistry Analyzer was used to determine the serum levels. The cut-off points of reference values were the 75th and 95th percentiles for total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) while the 25th and 5th percentiles were used for high-density lipoprotein cholesterol (HDL-C) concentrations. Results: The highest 95th percentiles of TC among the four groups were 5.34 mmol/L for boys and 5.11 mmol/L for girls. Compared with those of boys, female TG levels were obviously higher in the 10-14-year-old group (P < 0.05) and HDL-C levels were significantly higher in the 15-18-year-old group (P < 0.05). The serum TC, HDL-C, and LDL-C all peaked during the 6-9-year-old period and then declined during the adolescent stage. Also, the serum TG continuously increased with a relative plateau during the 6-14-year-old period. Obese and overweight children had higher TG and LDL-C levels but lower HDL-C levels. Conclusion: This study showed a picture of the serum lipids distribution in Chinese children and found that their TC levels were lower than those of children in Japan, Iran, and France, but were higher than those of Italian children. © 2010 Japan Pediatric Society.

Wei H.,Peking University | Zhang R.,Peking University | Jin H.,Peking University | Liu D.,Peking University | And 5 more authors.
Antioxidants and Redox Signaling | Year: 2010

The mechanisms responsible for the cardioprotective effect of hydrogen sulfide (H2S) are unclear. The present study was designed to examine whether H2S could regulate hyperhomocysteinemia (HHcy)-induced cardiomyocytic endoplasmic reticulum (ER) stress. A rat model of HHcy was produced, and H9c2 cells (rat embryonic heart-derived cell line) were cultured. The plasma homocysteine was measured by using HPLC. Plasma H2S concentration and myocardial H2S production were measured with a sulfide-sensitive electrode. Confocal immunofluorescent analysis for cardiomyocytic C/EBP homologous protein (CHOP) was performed. Glucose-regulated protein 78 (GRP78), CHOP, and caspase 12 expressions by myocardial tissues and cleaved caspase 12 and p-eIF2α expressions by H9c2 cells were detected with Western blotting. The results showed that methionine overload induced HHcy, resulting in a marked cardiomyocytic ER stress, whereas endogenous production of H2S was reduced in rats with HHcy. H2S supplementation, however, decreased expressions of ER stress-associated proteins, including GRP78, CHOP, and caspase 12, by myocardial tissues in vivo. The inhibition of endogenous H2S production further enhanced cardiomyocytic ER stress, but H2S supplementation effectively antagonized the H9c2 cell CHOP, cleaved caspase 12 and p-eIF2α expressions induced by Hcy, thapsigargin, or tunicamycin in vitro. The results suggest that H2S can attenuate cardiomyocytic ER stress in HHcy-induced cardiomyocytic injury. Antioxid. Redox Signal. 12, 0000-0000. © 2010, Mary Ann Liebert, Inc.

Zhang R.,Peking University | Sun Y.,Peking University | Tsai H.,Peking University | Tang C.,Peking University | And 4 more authors.
PLoS ONE | Year: 2012

Hydrogen sulfide (H2S) is a novel gasotransmitter that inhibits L-type calcium currents (ICa, L). However, the underlying molecular mechanisms are unclear. In particular, the targeting site in the L-type calcium channel where H2S functions remains unknown. The study was designed to investigate if the sulfhydryl group could be the possible targeting site in the L-type calcium channel in rat cardiomyocytes. Cardiac function was measured in isolated perfused rat hearts. The L-type calcium currents were recorded by using a whole cell voltage clamp technique on the isolated cardiomyocytes. The L-type calcium channel containing free sulfhydryl groups in H9C2 cells were measured by using Western blot. The results showed that sodium hydrosulfide (NaHS, an H2S donor) produced a negative inotropic effect on cardiac function, which could be partly inhibited by the oxidant sulfhydryl modifier diamide (DM). H2S donor inhibited the peak amplitude of ICa, L in a concentration-dependent manner. However, dithiothreitol (DTT), a reducing sulfhydryl modifier markedly reversed the H2S donor-induced inhibition of ICa, L in cardiomyocytes. In contrast, in the presence of DM, H2S donor could not alter cardiac function and L type calcium currents. After the isolated rat heart or the cardiomyocytes were treated with DTT, NaHS could markedly alter cardiac function and L-type calcium currents in cardiomyocytes. Furthermore, NaHS could decrease the functional free sulfhydryl group in the L-type Ca2+ channel, which could be reversed by thiol reductant, either DTT or reduced glutathione. Therefore, our results suggest that H2S might inhibit L-type calcium currents depending on the sulfhydryl group in rat cardiomyocytes. © 2012 Zhang et al.

Liang Y.,Peking University | Liu D.,Peking University | Ochs T.,Northwestern University | Tang C.,Peking University | And 8 more authors.
Laboratory Investigation | Year: 2011

Recently, sulfur dioxide (SO2) was discovered to be produced in the cardiovascular system and to influence important biological processes. Here, we investigated changes in endogenous SO2 /glutamic oxaloacetic transaminase (GOT) pathway in the development of isoproterenol (ISO)-induced myocardial injury in rats and the regulatory effect of SO2 on cardiac function, myocardial micro- and ultrastructure, and oxidative stress. Wistar male rats were divided into control, ISO-treated, ISO+SO2, and SO2 groups. At the termination of the experiment, parameters of cardiac function and hemodynamics were measured and the micro- and ultrastructure of myocardium and stereological ultrastructure of mitochondria were analyzed. Myocardial SO2 content was detected by high-performance liquid chromatography. GOT (key enzyme for endogenous SO 2 production) activity and gene (GOT1 and GOT2) expressions were measured, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), hydrogen peroxide, and superoxide radical levels were assayed. SOD (SOD1 and SOD2) and GSH-Px (GSH-Px1) gene expressions were also detected. The results showed that SO2 donor at a dose of 85 mg/(kg day) did not impact the cardiac function and structure of rats, but exerted a subtle influence on myocardial redox status. ISO-treated rats exhibited decreased cardiac function, damaged myocardial structures, and downregulated endogenous SO2 /GOT pathway. Meanwhile, myocardial oxidative stress increased, whereas antioxidative capacity downregulated. Administration of SO 2 markedly improved cardiac function and ISO-induced myocardial damage by ameliorating the pathological structure of the myocardium and the mitochondria. At the same time, myocardial products of oxidative stress decreased, whereas antioxidative capacity increased. These results suggest that downregulation of the endogenous SO 2 /GOT pathway is likely involved in the pathogenesis of ISO-induced myocardial injury. SO2 protects against ISO-induced myocardial injury associated with increased myocardial antioxidant capacity in rats. © 2011 USCAP, Inc All rights reserved.

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